Human CD4 and CD8 T Cell Responses to<i>Mycobacterium tuberculosis</i>: Antigen Specificity, Function, Implications and Applications

Ottenhoff, Tom H. M.; Lewinsohn, Deborah A.; Lewinsohn, David

doi:10.1002/9783527611614.ch23

Cited by 8 publications

(3 citation statements)

References 165 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…M1 macrophage phenotype is characterized by production of pro-inflammatory cytokines (tumor necrosis factor [TNF] α, IL-12), chemokines IL-8 and monocyte chemoattractant protein-1, and nitric oxide as well as biasing T cells toward the T H 1 phenotype and interferon (IFN) γ-producing CD8 + T cells ( 46 47 48 ). M1 effector functions against MTB include phagosome-lysosome fusion, autophagy, apoptosis, efferocytosis, and granuloma formation ( 49 50 ).…”

Section: The Effects Of Shs/direct Cs Exposure On Immune Cells Relevamentioning

confidence: 99%

“…MTB -specific T H 1 cells (IL-12 + , IFNγ + , TNFα + ) stimulate inflammation, help skew macrophages to the M1 phenotype, and initiate antibacterial effector functions in infected macrophages ( 85 86 ). Early expansion of T H 2 cells (IL-4 + , IL-13 + ) antagonizes protective cellular immunity, resulting in a partial or complete loss of TB control ( 46 87 88 ). T H 17 cells (IL-17 + , IL-22 + ) recruit neutrophils through the chemoattractant actions of IL-17, resulting in improved early granuloma formation and increased cooperation between neutrophils and macrophages in killing MTB ( 89 ).…”

Section: The Effects Of Shs/direct Cs Exposure On Immune Cells Relevamentioning

confidence: 99%

“…CD8 + T cells are also required for optimal host defense against human MTB disease ( 46 97 ). CD8 + T cells recognize protein and lipid antigens that are either class I MHC or CD1 restricted, respectively ( 98 99 ).…”

Section: The Effects Of Shs/direct Cs Exposure On Immune Cells Relevamentioning

confidence: 99%

See 2 more Smart Citations

Epidemiologic Evidence of and Potential Mechanisms by Which Second-Hand Smoke Causes Predisposition to Latent and Active Tuberculosis

Bai¹,

Aerts

Verma

et al. 2018

Immune Netw

View full text Add to dashboard Cite

Many studies have linked cigarette smoke (CS) exposure and tuberculosis (TB) infection and disease although much fewer have studied second-hand smoke (SHS) exposure. Our goal is to review the epidemiologic link between SHS and TB as well as to summarize the effects SHS and direct CS on various immune cells relevant for TB. PubMed searches were performed using the key words “tuberculosis” with “cigarette,” “tobacco,” or “second-hand smoke.” The bibliography of relevant papers were examined for additional relevant publications. Relatively few studies associate SHS exposure with TB infection and active disease. Both SHS and direct CS can alter various components of host immunity resulting in increased vulnerability to TB. While the epidemiologic link of these 2 health maladies is robust, more definitive, mechanistic studies are required to prove that SHS and direct CS actually cause increased susceptibility to TB.

show abstract

Section: The Effects Of Shs/direct Cs Exposure On Immune Cells Relevamentioning

confidence: 99%

Section: The Effects Of Shs/direct Cs Exposure On Immune Cells Relevamentioning

confidence: 99%

See 1 more Smart Citation

Epidemiologic Evidence of and Potential Mechanisms by Which Second-Hand Smoke Causes Predisposition to Latent and Active Tuberculosis

Bai¹,

Aerts

Verma

et al. 2018

Immune Netw

View full text Add to dashboard Cite

show abstract

Autophagy in Immunity Against Mycobacterium tuberculosis: a Model System to Dissect Immunological Roles of Autophagy

Deretić

Delgado

Vergne

et al. 2009

Current Topics in Microbiology and Immunology

103

View full text Add to dashboard Cite

The recognition of autophagy as an immune mechanism has been affirmed in recent years. One of the model systems that has helped in the development of our current understanding of how autophagy and more traditional immunity systems cooperate in defense against intracellular pathogens is macrophage infection with Mycobacterium tuberculosis. M. tuberculosis is a highly significant human pathogen that latently infects billions of people and causes active disease in millions of patients worldwide. The ability of the tubercle bacillus to persist in human populations rests upon its macrophage parasitism. One of the initial reports on the ability of autophagy to act as a cellautonomous innate immunity mechanism capable of eliminating intracellular bacteria was on M. tuberculosis. This model system has further contributed to the recognition of multiple connections between conventional immune regulators and autophagy. In this chapter, we will review how these studies have helped to establish the following principles: (1) autophagy functions as an innate defense mechanism against intracellular microbes; (2) autophagy is under the control of pattern recognition receptors (PRR) such as Toll-like receptors (TLR), and it acts as one of the immunological output effectors of PRR and TLR signaling; (3) autophagy is one of the effector functions associated with the immunity-regulated GTPases, which were initially characterized as molecules involved in cellautonomous defense, but whose mechanism of function was unknown until recently; (4) autophagy is an immune effector of Th1/Th2 T cell response polarization-autophagy is activated by Th1 cytokines (which act in defense against intracellular pathogens) and is inhibited by Th2 cytokines (which make cells accessible to intracellular pathogens). Collectively, the studies employing the M. tuberculosis autophagy model system have contributed to the development of a more comprehensive view of autophagy as an immunological process. This work and related studies by others have led us to propose a model of how autophagy, an ancient innate immunity defense, became integrated over the course of evolution with other immune mechanisms of ever-increasing complexity.

show abstract

Cationic pH-sensitive liposome-based subunit tuberculosis vaccine induces protection in mice challenged with Mycobacterium tuberculosis

Szachniewicz,

van den Eeden,

van Meijgaarden

et al. 2024

European Journal of Pharmaceutics and Biopharmaceutics

View full text Add to dashboard Cite

Human CD4 and CD8 T Cell Responses toMycobacterium tuberculosis: Antigen Specificity, Function, Implications and Applications

Cited by 8 publications

References 165 publications

Epidemiologic Evidence of and Potential Mechanisms by Which Second-Hand Smoke Causes Predisposition to Latent and Active Tuberculosis

Epidemiologic Evidence of and Potential Mechanisms by Which Second-Hand Smoke Causes Predisposition to Latent and Active Tuberculosis

Autophagy in Immunity Against Mycobacterium tuberculosis: a Model System to Dissect Immunological Roles of Autophagy

Cationic pH-sensitive liposome-based subunit tuberculosis vaccine induces protection in mice challenged with Mycobacterium tuberculosis

Contact Info

Product

Resources

About